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Search results for: cytokines

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#32474962   2020/05/30 To Up

Pretreatment with Retro-2 protects cells from death caused by ricin toxin by retaining the capacity of protein synthesis.

The current study explores the detoxification effect of Retro-2 on ricin toxin (RT) cytotoxicity, as well as the mechanisms underlying such effects, to provide a basis for follow-up clinical applications of Retro-2. The mouse-derived mononuclear/macrophage cell line, RAW264.7, was used to evaluate the detoxification effect of Retro-2 on RT by detecting cell viability, capacity for protein synthesis and the expression of cytokines, as well as endoplasmic reticulum stress (ERS)-related mRNA. The results indicated that many cells died when challenged with concentrations of RT ≥50ng/mL. The protein synthesis capacity of cells decreased when challenged with 200ng/mL RT for 2hours. Furthermore, the synthesis and release of many cytokines decreased, while the expression of cytokines or ERS-related mRNA increased when challenged with 200ng/mL of RT for 12 or more hours. However, cell viability, capacity for protein synthesis and release levels of many cytokines were higher, while the expression levels of cytokine, or ERS-related mRNA, were lower in cells pretreated with 20μm Retro-2 and challenged with RT, compared with those that had not been pretreated with Retro-2. In conclusion, Retro-2 retained the capacity for protein synthesis inhibited by RT, alleviated ERS induced by RT and increased the viability of cells challenged with RT. Retro-2 shows the potential for clinical applications.
Zhouguang Jiao, Yuehua Ke, Sha Li, Duo Su, Changjiao Gan, Lingfei Hu, Xiaodong Zhao, Bo Gao, Yajun Song, Dongsheng Zhou, Yefeng Qiu, Huiying Yang

2106 related Products with: Pretreatment with Retro-2 protects cells from death caused by ricin toxin by retaining the capacity of protein synthesis.

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#32474935   2020/05/31 To Up

Soft tissue healing around platform-switching and platform-matching single implants: A randomized clinical trial.

Implants with platform-switching (PS) design have been demonstrated to reduce marginal bone loss. However, the influence on peri-implant soft tissue healing is unclear. This study was designed to investigate its effect on peri-implant soft tissue healing after implant uncovery.
Guo-Liang Cheng, Binnaz Leblebicioglu, Jianrong Li, Hua-Hong Chien

2003 related Products with: Soft tissue healing around platform-switching and platform-matching single implants: A randomized clinical trial.



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#32474927   2020/05/31 To Up

The proinflammatory cytokines IL-1β and TNF-α modulate corneal epithelial wound healing through p16 suppressing STAT3 activity.

The proinflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) are involved in the corneal inflammatory response and wound healing following corneal injuries. However, the mechanism by which proinflammatory cytokines modulate corneal epithelial wound healing remains unclear. In this study, we found that IL-1β or TNF-α was transiently elevated during corneal epithelial wound healing in mice. After corneal epithelial debridement, persistent treatment with IL-1β or TNF-α restrained the level of phosphorylated signal transducer and activator of transcription 3 (p-STAT3) and boosted the level of cell cycle inhibitor p16 , resulting in impaired corneal epithelial repair. When p16 was deleted, the p-STAT3 level in corneal epithelium was enhanced and corneal epithelial wound healing was clearly accelerated. In diabetic mice, IL-1β, TNF-α, and p16 appeared a sustained and strong expression in the corneal epithelium, and p16 knockdown partially reverted the defective diabetic corneal epithelial repair. Furthermore, immunoprecipitation proved that p16 interacted with p-STAT3 and thus possibly suppressed the STAT3 activity. Our findings revealed a novel mechanism that the proinflammatory cytokines modulate corneal epithelial wound healing via the p16 -STAT3 signaling.
Xiaolei Wang, Songmei Zhang, Muchen Dong, Yunqiu Li, Qingjun Zhou, Lingling Yang

2622 related Products with: The proinflammatory cytokines IL-1β and TNF-α modulate corneal epithelial wound healing through p16 suppressing STAT3 activity.

2 Membrane supply100 assays1 mg96 Wells/Kitmin 2 cartons50 ug2 Membrane supply100 assays25 100.00 ul

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#32474876   // To Up

Long-Term Ex Vivo Expansion of Murine Spermatogonial Stem Cells in a Simple Serum-Free Medium.

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Hiroshi Kubota, Kazue Kakiuchi

1249 related Products with: Long-Term Ex Vivo Expansion of Murine Spermatogonial Stem Cells in a Simple Serum-Free Medium.

1.00 flask100 μg100.00 ug100 μg100 μg100 extractions1 mg1 mg 0.1 mg

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#32474766   2020/05/30 To Up

Gene polymorphisms of pro-inflammatory cytokines may affect the risk of Graves' disease: a meta-analysis.

Gene polymorphisms of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1) and interleukin-6 (IL-6) may influence the risk of Graves' disease, but the results of so far published studies remain inconclusive. Therefore, the authors conducted this meta-analysis to assess relationships between TNF-α/IL-1/IL-6 polymorphisms and the risk of Graves' disease by pooling the findings of all relevant studies.
P Zhu, X Wu, J Zhou, K Wu, Y Lu

1587 related Products with: Gene polymorphisms of pro-inflammatory cytokines may affect the risk of Graves' disease: a meta-analysis.

2 Membrane supply50 ug1 module50 ug16 Arrays/Slide1 ml100ug5ug50 ug

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#32474680   2020/05/30 To Up

Exendin-4 Attenuates Remodeling in the Remote Myocardium of Rats After an Acute Myocardial Infarction by Activating β-Arrestin-2, Protein Phosphatase 2A, and Glycogen Synthase Kinase-3 and Inhibiting β-Catenin.

This study tested if the protective anti-remodeling effect of GLP-1 agonist Exendin-4 after an acute myocardial infarction (MI) in rats involves inhibition of the Wnt1/β-catenin signaling pathway.
Refaat A Eid, Mohammad Adnan Khalil, Mahmoud A Alkhateeb, Samy M Eleawa, Mohamed Samir Ahmed Zaki, Attalla Farag El-Kott, Mubarak Al-Shraim, Fahmy El-Sayed, Muhammad Alaa Eldeen, Mashael Mohammed Bin-Meferij, Khalid M E Awaji, Abdullah S Shatoor

2729 related Products with: Exendin-4 Attenuates Remodeling in the Remote Myocardium of Rats After an Acute Myocardial Infarction by Activating β-Arrestin-2, Protein Phosphatase 2A, and Glycogen Synthase Kinase-3 and Inhibiting β-Catenin.

100ul100μg10 mg10 mg1000 TESTS/0.65ml100 mg5mg2.5 mg1 Set1 Set1 Set1 Set

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#32474610   2020/05/31 To Up

Homeostatic state of microglia in a rat model of chronic sleep restriction.

Chronic sleep restriction (CSR) negatively impacts brain functions. Whether microglia, the brain's resident immune cells, play any role is unknown. We studied microglia responses to CSR using a rat model featuring slowly rotating wheels (3 h on/1 h off), which was previously shown to induce both homeostatic and adaptive responses in sleep and attention. Adult male rats were sleep restricted for 27 or 99 h. Control rats were housed in locked wheels. After 27 and/or 99 h of CSR, the number of cells immunoreactive for the microglia marker ionized calcium-binding adaptor molecule-1 (Iba1) and the density of Iba1 immunoreactivity were increased in 4/10 brain regions involved in sleep/wake regulation and cognition, including the prelimbic cortex, central amygdala, perifornical lateral hypothalamic area, and dorsal raphe nucleus. CSR neither induced mitosis in microglia (assessed with bromodeoxyuridine) nor impaired blood-brain barrier permeability (assessed with Evans Blue). Microglia appeared ramified in all treatment groups and, when examined quantitatively in the prelimbic cortex, their morphology was not affected by CSR. After 27 h, but not 99 h, of CSR, mRNA levels of the anti-inflammatory cytokine interleukin-10 were increased in the frontal cortex. Pro-inflammatory cytokine mRNA levels (tumor necrosis factor-α, interleukin-1β, and interleukin-6) were unchanged. Furthermore, cortical microglia were not immunoreactive for several pro- and anti-inflammatory markers tested, but were immunoreactive for the purinergic P2Y12 receptor. These results suggest that microglia respond to CSR while remaining in a physiological state and may contribute to the previously reported homeostatic and adaptive responses to CSR.
Shannon Hall, Samüel Deurveilher, George S Robertson, Kazue Semba

1800 related Products with: Homeostatic state of microglia in a rat model of chronic sleep restriction.

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#32474541   // To Up

Plasma levels of tumor necrosis factor-alpha, interferon-gamma, inducible nitric oxide synthase, and 3-nitrotyrosine in drug-resistant and drug-sensitive pulmonary tuberculosis patients, Ibadan, Nigeria.

Nigeria is one of the countries with a high burden of tuberculosis (TB) in the world. TB associated inflammation is reported to be central to progression from latent TB to active TB or drug sensitive TB (DSTB) to drug resistant TB (DRTB). Inflammatory cytokines, especially interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α), act synergistically in the control of TB infection. They activate macrophages to produce effector molecules such as inducible nitric oxide synthase (iNOS), nitric oxide, and ultimately 3-nitrotyrosines(3-NTs), which are involved in the control of TB. This study investigated the potential involvement of TNF-α, IFN-γ, iNOS, and 3-NT in differentiating DRTB and DSTB in Ibadan, Nigeria.
Elizabeth Bosede Bolajoko, Olatunbosun Ganiyu Arinola, Georgina Njideka Odaibo, Mamoudou Maiga

1480 related Products with: Plasma levels of tumor necrosis factor-alpha, interferon-gamma, inducible nitric oxide synthase, and 3-nitrotyrosine in drug-resistant and drug-sensitive pulmonary tuberculosis patients, Ibadan, Nigeria.

100 96tests10ug0.1 mg5ug96T1 kit(96 Wells) 96T/Kit 1 kit(96 Wells)5ug20 25

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#32474414   // To Up

CD40 agonist-induced IL-12p40 potentiates hepatotoxicity.

CD40 is a compelling target for cancer immunotherapy, however, attempts to successfully target this pathway have consistently been hampered by dose-limiting toxicity issues in the clinic that prevents the administration of efficacious doses.
Caroline Bonnans, Graham Thomas, Wenqian He, Breanna Jung, Wei Chen, Min Liao, Jonathan Heyen, Bernard Buetow, Smitha Pillai, Diane Matsumoto, Javier Chaparro-Riggers, Shahram Salek-Ardakani, Yan Qu

1760 related Products with: CD40 agonist-induced IL-12p40 potentiates hepatotoxicity.

5 mg10 μg200.00 ug50 ul1 mg1 mg100ug250 100 10ug250.1 mg

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